Development of a new temporary luting agent consisting of PEMA and eugenol--residue ratio and bond strength of luting cements for abutment materials.

PEMA- and eugenol-based trial agents (PE 1.0, PE 1.6) possessed the requisite dental engineering properties that satisfied the requirements for temporary luting agents. To assess their clinical applicability, this study examined the following properties after the trial agents were removed: their residue ratios on the abutment surface and the bond strengths of resin-modified glass ionomer cement and resin cement for the abutment materials. The residue ratio of PE 1.0 on the abutment material after temporary restoration removal was lower than those of comparable temporary luting agents (polycarboxylate cement type, zinc oxide-eugenol cement type), and no residue was recognized for PE 1.6. On bond strength, those of the resin-modified glass ionomer cement and resin cement for the resin core and bovine dentin surface after the removal of trial agents tended to be the same or increase in comparison to commercial temporary luting agents. In conclusion, results of this study suggested that the trial agents were suitable for clinical use.

Copper- and iron-rich matrices in hepatocellular lipofuscin particles of a young male patient: diagnostic ultrastructures for Wilson disease.

A 17-year-old male patient appeared with the biochemical liver damage associated with hypoceruloplasminemia and mild iron overload. Genetic analysis identified a compound heterozygosity of ATP7B responsible for the primary copper toxicosis of Wilson disease without mutations in HFE. A liver specimen consisted of cirrhotic nodules of large-sized hepatocytes with fatty change and those of fat-free small-sized hepatocytes. Histochemically, iron was distributed diffusely in the small-sized hepatocytes, while copper grains appeared in a few of the hepatocytes near the fibrous bands. X-ray microanalysis on the liver tissue fixed with a 0.1% osmium tetroxide solution and embedded in epoxy resin disclosed (1) complex formation of copper with sulfur, and iron with phosphorus in the hepatocyte lipofuscin particles, (2) intraparticle localization of the cuprothionein in the less dense matrix and ferric proteins in the dense matrix, and (3) high affinity of the cuprothionein to lead staining. Considering the fact that ceruloplasmin is the major ferroxidase essential for iron efflux, iron deposits in the hypoceruloplasminemic patients with Wilson disease are not a complication, but a natural event. This study disclosed for the first time the diagnostic ultrastructures of Wilson disease, which might represent different detoxification processes to the reactive metals of copper and iron.

Genetic background of primary iron overload syndromes in Japan.

The different prevalences of iron overload syndromes between Caucasians and Asians may be accounted for by the differences in genetic background. The major mutation of hemochromatosis in Celtic ancestry, C282Y of HFE, was reported in a Japanese patient. Five patients of 3 families with the hepatic transferrin receptor gene (TFR2)-linked hemochromatosis were found in different areas of Japan, suggesting that TFR2 is a major gene in Japanese people. Three patients with mutations in the hemojuvelin gene, HJV, showed also middle-age-onset hemochromatosis. A heterozygous mutation in the H ferritin gene, FTH1, was found in a family of 3 affected patients. Another autosomal dominant SLC40A1-linked hyperferritinemia (ferroportin disease) was found in 3 patients of 2 families. Two patients with hemochromatosis were free from any mutations in the genes investigated. In conclusion, the genetic backgrounds of Japanese patients with primary iron overload syndromes were partially clarified, showing some phenotype-genotype correlations.